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Chapter 34 : Adherence and Colonization

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Abstract:

This chapter focuses on host, environmental, and bacterial factors that contribute to the establishment and persistence of within the stomach rather than on genes for products that specifically contribute to host damage. Epidemiological studies indicate transmission occurs most often during early childhood, with the mother as the most common source of infection. exhibits both host tropism, colonizing only primates, and tissue tropism, adhering only to the gastric epithelial lining of the antrum or staying in the gastric mucous layer. Adhesion is considered to be necessary for the establishment of infection, but many other factors also influence the persistence of in the gastric mucosa. Adhesins are bacterial proteins, glycoconjugates, or lipids that are involved in the initial stages of colonization by mediating the interaction between the bacterium and the host cell surface. Acidity could be a signal for enhanced adhesin transcriptional or translational expression, or could simply favor adhesin-receptor interactions. Chronic infection modulates the balance between gastric epithelial cell proliferation (cancer) and epithelial cell death (apoptosis). Adherence of to human cells correlates well with the amount of phosphatidylethanolamine (PE) present in lipids extracted from these host cells. Heat shock proteins of have surprisingly been shown by numerous laboratories to be surface exposed and involved in adherence. Colonization by has only been confirmed in the gastric mucosa.

Citation: Testerman T, McGee D, Mobley H. 2001. Adherence and Colonization, p 381-417. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch34

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Figures

Image of Figure 1
Figure 1

Schematic representation of gastric structure. The stomach is divided into four regions—the cardia, fundus, body, and antrum. The gastric epithelium is coated by a protective layer of mucus seceted by specialized epithelial cells. Gastric pits contain several cell types, including mucus-secreting cells and enteroendocrine cells. The array of cell types found in individual gastric pits varies in different regions of the stomach. colonization is largely confined to the antrum, which lacks acid-secreting parietal cells.

Citation: Testerman T, McGee D, Mobley H. 2001. Adherence and Colonization, p 381-417. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch34
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Image of Figure 2
Figure 2

Overview of adherence phenotypes of . adheres to the host cell surface via bacterial adhesins interacting with host cell receptors (see Fig. 4 ). Following attachment, microvilli are denuded and tight junctions disrupted. Bacterial urease is at least partially responsible for tight junction disruption, but VacA may also be involved. It is not clear when mucus granules are depleted in relation to the other phenotypes, and at what stage rare bacteria become internalized. Additionally, bacterial genes involved in the steps immediately after adherence are poorly understood, so it is not yet possible to block any of these steps so that they can be examined in more detail. The only genes implicated in any of the steps immediately after adherence are those in the cag pathogenicity island. In the model presented, translocation and tyrosine phosphorylation of CagA occurs after the pedestal formation, but it is also possible that this happens before pedestal formation.

Citation: Testerman T, McGee D, Mobley H. 2001. Adherence and Colonization, p 381-417. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch34
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Figure 3

Interactions of with mucin. chemotactically moves from a region of low concentration of mucin to a higher concentration and then binds to it. There may be competition between Nap binding to mucin (left pathway) and LPS interacting with the host mucin receptor, which would block the ability of mucin to bind its own receptor (right pathway). mucinase activity degrades mucin either by removing sulfate residues (desulfation) or by cleaving the proteinaceous component of mucin (proteolysis). This allows access to receptors on the host cell, leading to tighter adherence. Following adherence, mucin-containing granules are depleted, so that mucin release is perturbed. This leads to decreased mucin concentration in the mucous layer and would allow additional to bind to gastric epithelial cells. There are very likely other adhesins that interact with mucin, since mucin has a diverse repertoire of glycoconjugate moieties.

Citation: Testerman T, McGee D, Mobley H. 2001. Adherence and Colonization, p 381-417. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch34
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Figure 4

Interaction of adhesins with host cell receptors. For simplicity, only the best studied adhesin-receptor interactions are shown. The in vivo situation is likely much more complex, as described in the text, in that there may be dynamic and temporal expression of adhesins and receptors, and during any given time, may interact with only a subset of the cellular receptors. (A) Interaction of adhesins to gastric epithelial cell receptors. (B) Interaction of adhesins to the basement membrane protein laminin. has evolved multiple mechanisms to interact with host laminin.

Citation: Testerman T, McGee D, Mobley H. 2001. Adherence and Colonization, p 381-417. In Mobley H, Mendz G, Hazell S (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555818005.ch34
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